乳糖操纵子的分解代谢物阻遏。乳糖启动子突变的影响。

Catabolite repression of the lac operon. Effect of mutations in the lac promoter.

作者信息

Yudkin M D

出版信息

Biochem J. 1970 Aug;118(5):741-6. doi: 10.1042/bj1180741.

DOI:10.1042/bj1180741

PMID:4920388

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1179282/

Abstract

Several lac diploid strains of Escherichia coli were constructed and tested to discover whether mutations in the lac promoter alleviate catabolite repression. 2. In each of these diploids the chromosome carries one of the promoter mutations, L8, L29 or L1; so that the rate of synthesis of the enzymes of the lac operon is only 2-6% of the fully induced wild-type. Each diploid harbours the episome F'lacM15 that specifies the synthesis of thiogalactoside transacetylase under the control of intact regulator, promoter and operator regions, but has a deletion in the structural gene for beta-galactosidase. In each diploid more than 90% of the thiogalactoside transacetylase is synthesized from the episome, and 100% of the beta-galactosidase is synthesized from the chromosome, and comparison of the extent of catabolite repression that the two enzymes suffered indicated whether the chromosomal promoter mutation relieves catabolite repression. 3. In the strains in which the promoter carries either of the point mutations L8 or L29 the enzymes were equally repressed, suggesting that neither L8 nor L29 affects catabolite repression. 4. In a diploid strain harbouring the same episome but carrying deletion L1 on the chromosome, synthesis of beta-galactosidase suffered much less repression than that of thiogalactoside transacetylase. 5. In a diploid strain in which the chromosome carries L1 and also a second mutation that increases the rate of expression of lac to that permitted by L8 or L29, the synthesis of beta-galactosidase again suffered much less repression than the synthesis of thiogalactoside transacetylase. 6. The effect of L1 (which deletes the boundary between the i gene and the lac promoter) is ascribed to its bringing the expression of lac under the control of the promoter of the i gene. 7. Even in strains carrying L1, some catabolite repression persists; this is not due to a trans effect from the episome since it occurs equally in a haploid strain with L1.

摘要

构建并测试了几种大肠杆菌的乳糖操纵子部分二倍体菌株，以探究乳糖启动子中的突变是否能缓解分解代谢物阻遏。2. 在这些二倍体中，每一个的染色体都携带一种启动子突变，即L8、L29或L1；因此，乳糖操纵子酶的合成速率仅为完全诱导的野生型的2%-6%。每个二倍体都携带附加体F'lacM15，它在完整的调节基因、启动子和操纵区的控制下指定硫代半乳糖苷转乙酰酶的合成，但β-半乳糖苷酶的结构基因有缺失。在每个二倍体中，超过90%的硫代半乳糖苷转乙酰酶是由附加体合成的，100%的β-半乳糖苷酶是由染色体合成的，通过比较这两种酶所遭受的分解代谢物阻遏程度，可表明染色体启动子突变是否能缓解分解代谢物阻遏。3. 在启动子携带点突变L8或L29的菌株中，这两种酶受到的阻遏程度相同，这表明L8和L29都不影响分解代谢物阻遏。4. 在一个携带相同附加体但染色体上有缺失L1的二倍体菌株中，β-半乳糖苷酶的合成受到的阻遏比硫代半乳糖苷转乙酰酶少得多。5. 在一个染色体携带L1且还有另一个将乳糖表达速率提高到L8或L29所允许水平的突变的二倍体菌株中，β-半乳糖苷酶的合成再次比硫代半乳糖苷转乙酰酶受到的阻遏少得多。6. L1（它删除了i基因和乳糖启动子之间的边界）的作用被归因于它使乳糖的表达受i基因启动子的控制。7. 即使在携带L1的菌株中，仍存在一些分解代谢物阻遏；这不是由于来自附加体的反式作用，因为在有L1的单倍体菌株中也同样存在。